Initial exposure to a wide range of stressful situations can result in alterations in sensitivity to pain which outlast the exposure. Stress can induce not only analgesia, but also hyperalgesia. Certain stressors may even induce both analgesia and hyperalgesia in the same organism, although to different types of noxious stimuli. Repeated exposures to stress result in a progressive decline of the analgesic response, in much the same manner that the pituitary-adrenal responses to stress show adaptation. However, not all stressors induce analgesia, including some that produce maximal elevations in plasma levels of beta-endorphin, ACTH and adrenal corticosteroids. Some stressors induce analgesia that is reversed by the opiate antagonist drug, naloxone. Others cause a non-naloxone sensitive form of analgesia. The proposed set of psychophysical experiments will determine whether the sensory changes induced by stress are specific to the modality of pain, or whether they are accompanied by deficits in auditory and/or visual acuity as well. Sensory thresholds will be measured in animals by a reflex startle procedure in which weak sensory stimuli can inhibit the startle response if they occur slightly before the startle-eliciting stimulus. An interlocking set of experiments will also attempt to identify the behavioral factors that distinguish opioid (naloxone-sensitive) from nonopioid forms of stress-analgesia. The general case of the hypothesis to be tested is that opioid forms of analgesia, whether induced by stress or by drugs, may be accompanied by a concurrent state of hyperresponsivity to certain non-noxious stimuli. The relation between stress-induced analgesia and stress-induced hyperalgesia will also be analyzed, as will their neuroendocrine mechanisms. Finally, an attempt will be made to develop a new analgesimetric test, based upon the startle inhibition paradigm, which would not confound analgesia with a decreased capacity to execute a motor response, as current tests do.